A T helper 1 (Th1)-type immune response associated with interferon (IFN)-γ prevents remodeling and progression to DCM after myocarditis, while Th2- (IL-4 and IL-33-associated cytokines) and Th17-type (IL-17A and IL-6-associated cytokines) immune responses promote remodeling, fibrosis and DCM in mouse models and human studies [68,102,103,104,105,106,107,108,109]. The gene discussed is IL33; the disease is familial dilated cardiomyopathy.